Record Information |
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Version | 2.0 |
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Creation Date | 2009-06-19 21:58:26 UTC |
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Update Date | 2014-12-24 20:23:23 UTC |
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Accession Number | T3D1207 |
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Identification |
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Common Name | Copper(II) bromide |
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Class | Small Molecule |
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Description | Copper(II) bromide is a bromide of copper. It is used in photographic processing as an intensifier and as a brominating agent in organic synthesis. Copper is a chemical element with the symbol Cu and atomic number 29. Copper is an essential elements in plants and animals as it is required for the normal functioning of more than 30 enzymes. It occurs naturally throughout the environment in rocks, soil, water, and air. Bromine is a halogen element with the symbol Br and atomic number 35. Diatomic bromine does not occur naturally, but bromine salts can be found in crustal rock. (14, 8, 9, 12) |
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Compound Type | - Bromide Compound
- Copper Compound
- Industrial/Workplace Toxin
- Inorganic Compound
- Synthetic Compound
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Chemical Structure | |
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Synonyms | Synonym | Copper bromide (CuBr2) | Copper dibromide | Cupric bromide |
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Chemical Formula | Br2Cu |
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Average Molecular Mass | 223.354 g/mol |
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Monoisotopic Mass | 220.766 g/mol |
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CAS Registry Number | 7789-45-9 |
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IUPAC Name | dibromocopper |
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Traditional Name | dibromocopper |
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SMILES | Br[Cu]Br |
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InChI Identifier | InChI=1S/2BrH.Cu/h2*1H;/q;;+2/p-2 |
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InChI Key | InChIKey=QTMDXZNDVAMKGV-UHFFFAOYSA-L |
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Chemical Taxonomy |
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Description | belongs to the class of inorganic compounds known as transition metal bromides. These are inorganic compounds in which the largest halogen atom is Bromine, and the heaviest metal atom a transition metal. |
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Kingdom | Inorganic compounds |
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Super Class | Mixed metal/non-metal compounds |
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Class | Transition metal salts |
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Sub Class | Transition metal bromides |
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Direct Parent | Transition metal bromides |
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Alternative Parents | |
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Substituents | - Transition metal bromide
- Inorganic salt
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Molecular Framework | Not Available |
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External Descriptors | Not Available |
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Biological Properties |
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Status | Detected and Not Quantified |
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Origin | Exogenous |
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Cellular Locations | |
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Biofluid Locations | Not Available |
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Tissue Locations | Not Available |
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Pathways | Not Available |
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Applications | Not Available |
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Biological Roles | Not Available |
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Chemical Roles | Not Available |
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Physical Properties |
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State | Solid |
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Appearance | Black powder. |
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Experimental Properties | Property | Value |
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Melting Point | Not Available | Boiling Point | Not Available | Solubility | Not Available | LogP | Not Available |
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Predicted Properties | |
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Spectra |
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Spectra | Spectrum Type | Description | Splash Key | Deposition Date | View |
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Predicted LC-MS/MS | Predicted LC-MS/MS Spectrum - 10V, Positive | splash10-00di-0090000000-2fd11a8d8ba8d28e7f35 | 2016-08-03 | View Spectrum | Predicted LC-MS/MS | Predicted LC-MS/MS Spectrum - 20V, Positive | splash10-00di-0090000000-2fd11a8d8ba8d28e7f35 | 2016-08-03 | View Spectrum | Predicted LC-MS/MS | Predicted LC-MS/MS Spectrum - 40V, Positive | splash10-00di-0090000000-2fd11a8d8ba8d28e7f35 | 2016-08-03 | View Spectrum | Predicted LC-MS/MS | Predicted LC-MS/MS Spectrum - 10V, Negative | splash10-014i-0090000000-49f2eb0fa0f50ef70cfe | 2016-08-03 | View Spectrum | Predicted LC-MS/MS | Predicted LC-MS/MS Spectrum - 20V, Negative | splash10-014i-0090000000-49f2eb0fa0f50ef70cfe | 2016-08-03 | View Spectrum | Predicted LC-MS/MS | Predicted LC-MS/MS Spectrum - 40V, Negative | splash10-014i-0090000000-49f2eb0fa0f50ef70cfe | 2016-08-03 | View Spectrum |
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Toxicity Profile |
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Route of Exposure | Oral (8) ; inhalation (8) ; dermal (8) |
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Mechanism of Toxicity | Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. Bromine is a powerful oxidizing agent and is able to release oxygen free radicals from the water in mucous membranes. These free radicals are also potent oxidizers and produce tissue damage. In additon, the formation of hydrobromic and bromic acids will result in secondary irritation. The bromide ion is also known to affect the central nervous system, causing bromism. This is believed to be a result of bromide ions substituting for chloride ions in the in actions of neurotransmitters and transport systems, thus affecting numerous synaptic processes. (15, 16, 3, 8, 5, 1, 11) |
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Metabolism | Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. Bromine is mainly absorbed via inhalation, but may also enter the body through dermal contact. Bromine salts can be ingested. Due to its reactivity, bromine quickly forms bromide and may be deposited in the tissues, displacing other halogens. (15, 8, 10) |
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Toxicity Values | LD50: 536 mg/kg (Oral, Rat) (13) |
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Lethal Dose | 10 to 20 grams for an adult human (copper salts). (4) |
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Carcinogenicity (IARC Classification) | No indication of carcinogenicity to humans (not listed by IARC). |
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Uses/Sources | Copper(II) bromide is used in photographic processing as an intensifier and as a brominating agent in organic synthesis. (12) |
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Minimum Risk Level | Acute Oral: 0.01 mg/kg/day (Copper) (7)
Intermediate Oral: 0.01 mg/kg/day (Copper) (7) |
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Health Effects | People must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can cause damage to your liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. Bromine vapour causes irritation and direct damage to the mucous membranes. Elemental bromine also burns the skin. The bromide ion is a central nervous system depressant and chronic exposure produces neuronal effects. This is called bromism and can result in central reactions reaching from somnolence to coma, cachexia, exicosis, loss of reflexes or pathologic reflexes, clonic seizures, tremor, ataxia, loss of neural sensitivity, paresis, papillar edema of the eyes, abnormal speech, cerebral edema, delirium, aggressiveness, and psychoses. (14, 15, 16, 9, 10) |
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Symptoms | Breathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. Bromine vapour causes irritation and direct damage to the mucous membranes. Symptoms include lacrimation, rhinorrhoea, eye irritation with mucous secretions from the oropharyngeal and upper airways, coughing, dyspnoea, choking, wheezing, epistaxis, and headache. The bromide ion is a central nervous system depressant producing ataxia, slurred speech, tremor, nausea, vomiting, lethargy, dizziness, visual disturbances, unsteadiness, headaches, impaired memory and concentration, disorientation and hallucinations. This is called bromism. (15, 16, 9, 10) |
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Treatment | EYES: irrigate opened eyes for several minutes under running water.
INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice.
SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention.
INHALATION: supply fresh air. If required provide artificial respiration. |
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Normal Concentrations |
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| Not Available |
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Abnormal Concentrations |
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| Not Available |
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External Links |
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DrugBank ID | Not Available |
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HMDB ID | Not Available |
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PubChem Compound ID | 24611 |
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ChEMBL ID | Not Available |
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ChemSpider ID | 23013 |
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KEGG ID | Not Available |
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UniProt ID | Not Available |
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OMIM ID | |
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ChEBI ID | Not Available |
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BioCyc ID | Not Available |
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CTD ID | C408079 |
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Stitch ID | Copper(II) bromide |
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PDB ID | Not Available |
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ACToR ID | Not Available |
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Wikipedia Link | Not Available |
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References |
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Synthesis Reference | Not Available |
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MSDS | T3D1207.pdf |
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General References | - Brewer GJ: A brand new mechanism for copper toxicity. J Hepatol. 2007 Oct;47(4):621-2. Epub 2007 Jul 23. [17697726 ]
- Bardsley PA, Howard P, DeBacker W, Vermeire P, Mairesse M, Ledent C, Radermecker M, Bury T, Ansquer J: Two years treatment with almitrine bismesylate in patients with hypoxic chronic obstructive airways disease. Eur Respir J. 1991 Mar;4(3):308-10. [1907566 ]
- Ziouzenkova O, Orasanu G, Sharlach M, Akiyama TE, Berger JP, Viereck J, Hamilton JA, Tang G, Dolnikowski GG, Vogel S, Duester G, Plutzky J: Retinaldehyde represses adipogenesis and diet-induced obesity. Nat Med. 2007 Jun;13(6):695-702. Epub 2007 May 27. [17529981 ]
- Baselt RC (2000). Disposition of Toxic Drugs and Chemicals in Man, 5th ed. Foster City, CA: Chemical Toxicology Institute.
- Baxter PJ, Adams PH, & Aw TC (2000). Hunter's Diseases of Occupations. 9th ed. New York, NY: Oxford University Press Inc.
- Golomb, BA (1999). A Review of the Scientific Literature As It Pertains to Gulf War Illnesses. Volume 2: Pyridostigmine Bromide. Washington, DC: RAND.
- ATSDR - Agency for Toxic Substances and Disease Registry (2001). Minimal Risk Levels (MRLs) for Hazardous Substances. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
- Wikipedia. Copper. Last Updated 29 May 2009. [Link]
- ATSDR - Agency for Toxic Substances and Disease Registry (2004). Toxicological profile for copper. U.S. Public Health Service in collaboration with U.S. Environmental Protection Agency (EPA). [Link]
- International Programme on Chemical Safety (IPCS) INCHEM (1998). Environmental Health Criteria for Copper. [Link]
- US Environmental Protection Agency (2008). Drinking Water Health Advisory for 2,4-Dinitrotoluene and 2,6-Dinitrotoluene. [Link]
- Wikipedia. Copper(II) bromide. Last Updated 13 March 2009. [Link]
- The Physical and Theoretical Chemistry Laboratory of Oxford University (2007). Material Safety Data Sheet (MSDS) for copper (II) bromide. [Link]
- Wikipedia. Bromine. Last Updated 9 June 2009. [Link]
- International Programme on Chemical Safety (IPCS) INCHEM (1992). Poison Information Monograph for Bromine. [Link]
- Wikipedia. Potassium bromide. Last Updated 9 June 2009. [Link]
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Gene Regulation |
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Up-Regulated Genes | Not Available |
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Down-Regulated Genes | Not Available |
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